An anaerobic spriochete, Treponema hyodysenteriae, has been characterized as the primary etiological agent in swine dysentery. Harris, D. L.; Glock, R. D.; Christensen, C. R.; and Kinyon, J. M.: Vet. Med./Small Animal Clin. 67:61 (1972); Taylor, D. J.; and Alexander, T. J. L.: Brit. Vet. J. 127:108 (1971). But relatively little is known about the immunology of swine dysentery although resistance to reinfection can be demonstrated in convalescent pigs. In 1976, Glock et al reported that parenteral vaccination of pigs with killed cells of a virulent isolate of T. hyodysenteriae provided a significant degree of protection against subsequent intragastric challenge with live virulent T. hyodysenteriae. Glock, R. D., Schwartz, K. J., and Harris, D. L., Proceedings, International Pig Veterinary Society Congress, June 1976, Ames, Iowa. The vaccine was given in six intravenous injections at 6-day intervals. This was the first reported success in immunizing swine against swine dysentery infection.
Hudson et al found that oral dosing of an attenuated strain of T. hyodysenteriae provided no protection against subsequent challenge. Hudson, M. J., Alexander, T. J. L., Lysons, R. J., Wellstead, P. D., Brit. Vet. J. (1974) 130:37. Subsequently, Hudson et al attempted to immunize pigs with live attenuated T. hyodysenteriae using a combination of oral dosing and parenteral inoculation. Hudson, M. J., Alexander, T. J. L., Lysons, R. J., Prescott, J. F., Res. Vet. Science (1976) 21:366. Oral doses were administered on three consecutive days, and after an interval of several days, intraperitoneal vaccinations were administered, which were followed after several more days with intramuscular vaccinations. The overall results of these tests were summarized as follows: "Although vaccination appeared to enhance immunity to swine dysentery, half of the vaccinated pigs developed the disease. This level of protection would be unlikely to be of practical value in the field."
Treponema hyodysenteriae is a true pathogen in the sense that in conventional pigs Koch's postulates have been fulfilled. Glock, R. D., and Harris, D. L., Vet. Med./Small Animal Clin. 67 (1972): 65-68; Kinyon, J. M., Harris, D. L. and Glock, R. D., Infect. Immun. 15 (1977): 638-646. The status of T. hyodysenteriae as a pathogen is further evidenced by the fact that herds of pigs exist which are free of swine dysentery and are also free of T. hyodysenteriae. Kinyon, J. M., Songer, J. G., Janc, M., and Harris, D. L., In Proceedings 19th Annual Amer. Assoc. of Vet. Lab. Diag. (1976): 65-74. By contrast, pigs from these same herds will develop signs and lesions of swine dysentery when orally inoculated with only T. hyodysenteriae. Kinyon, J. M., Harris, D. L., and Glock, R. D., Infec. and Immun. 15 (2), (1977): 638-646. However, T. hyodysenteriae appears to require elements of the normal colonic flora to exert its pathogenicity.
While swine dysentery infection can be reproduced in field-raised pigs by dosing them orally with pure cultures of Treponema hyodysenteriae, attempts to do so have failed until recently. In 1975, Meyer et al reported that swine dysentery was produced in gnotobiotic piglets by dosing them orally with T. hyodysenteriae together with 4 gram negative non-sporing rod-shaped anaerobes. Meyer, R. C., Simon, J., and Byerly, C. S., Vet. Path. 12, (1975): 46-54. The anaerobes were not specifically identified by Meyer et al, but they were tentatively designated as either species of Bacteroides or Fusobacteria. In further tests with gnotobiotic pigs, Harris et al found that lesions typical of acute swine dysentery were produced by intragastric inoculation of T. hyodysenteriae in combination with Bacteroides vulgatus, either alone or with Fusobacterium necrophorum. All bacteria were administered live. Harris, D. L., Alexander, T. J. L., Whipp, S. C., Robinson, I. M., Glock R. D., and Matthews, P. J., J. Amer. Vet. Med. Assoc. 172 (1978): 468-471. In field raised pigs, it would be expected that natural colonic flora would include B. vulgatus, F. necrophorum and similar bacteria so that T. hyodysenteriae can exert its pathogenicity, producing the swine dysentery infection.